F. Kolar et al., PRESSURE-OVERLOAD INDUCED IN NEWBORN RATS - EFFECTS ON LEFT-VENTRICULAR GROWTH, MORPHOLOGY, AND FUNCTION, Pediatric research, 43(4), 1998, pp. 521-526
Gradual pressure overload was induced by abdominal aortic constriction
in male rats on postnatal d 6 (AC6) or 2 (AC2). At the age of 8 wk, t
he systemic blood pressure was measured, and the contractile performan
ce of the left ventricle (LV) was assessed after acute ligation of the
ascending aorta in open chest anesthetized animals. The LV free wall
was used for the determination of collagen concentration and morphomet
ric analysis of cardiac myocytes and capillaries. Aortic constriction
resulted in LV hypertrophy, which was more pronounced in AC2 (by 71%)
as compared with AC6 (by 34%) groups and correlated closely with the d
egree of pressure overload (r = 0.88 and 0.80, respectively). The righ
t ventricular weight was increased by 13% in the AC2 group only. Contr
actile performance of the LV of aortic constricted rats was significan
tly higher before as well as after the acute load, but the average fun
ctional reserve was unchanged in both experimental groups. Although th
e maximum value of the rate of pressure development increased linearly
with the degree of ventricular hypertrophy in the AC6 group (r = 0.82
), a negative correlation was observed in the AC2 animals (r = -0.61).
The density of myocytes was decreased, and the calculated average myo
cyte cross-sectional area was increased in aortic constricted rats, bu
t the coronary capillary density and myocardial concentration of colla
gen remained constant. Thus, in spite of the larger cardiac growth res
ponse in the younger age group, the capillary proliferation and collag
en formation were proportional to the ventricular hypertrophy. Therefo
re. the degrees of overload and hypertrophy do not seem to be limiting
factors. Pressure overload induced in newborn rats can be a useful mo
del for the study of mechanisms that control either the growth and dif
ferentiation of myocardium soon after birth, as well as the transition
from compensated to decompensated hypertrophy at later stages.